Evidence map›Paper›PMID 38185452›Full record

ArticleMolecular metabolism2024

ATP7A-dependent copper sequestration contributes to termination of β-CATENIN signaling during early adipogenesis.

H Yang, E Kabin, Y Dong, X Zhang, M Ralle, S Lutsenko

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular metabolism, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
3.4field-weighted citation impact, top 8% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

5 citing papers in PubMed, 11 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 4 institutions in 2 countries.

H YangHelen Diller Family Comprehensive Cancer Center, University of California, San Francisco, CA, USA. Electronic address: haojun.yang@ucsf.edu.
E KabinDepartment of Chemistry and Biotechnology, Tallinn University of Technology, Akadeemia tee 15, 12618 Tallinn, Estonia; Department of Physiology, Johns Hopkins Medical Institutes, Baltimore, MD, USA.
Y DongDepartment of Physiology, Johns Hopkins Medical Institutes, Baltimore, MD, USA.
X ZhangDepartment of Physiology, Johns Hopkins Medical Institutes, Baltimore, MD, USA.
M RalleDepartment of Molecular Genetics, OHSU, Portland OR, USA.
S LutsenkoDepartment of Physiology, Johns Hopkins Medical Institutes, Baltimore, MD, USA. Electronic address: lutsenko@jhmi.edu.
Johns Hopkins University · USOregon Health & Science University · USTallinn University of Technology · EEUniversity of California, San Francisco · US

Funding

Translational Research Central ServicesP30CA006973 · NCI · JOHNS HOPKINS UNIVERSITY · PI ALAN KEITH MEEKER · 1985 to 2026
$208.6M
QAQC Johns Hopkins Institute for Clinical and Translational ResearchUL1TR003098 · NCATS · JOHNS HOPKINS UNIVERSITY · PI FORD, DANIEL ERNEST · 2019 to 2023
$57.7M
Translational Research Enhancement CoreP30DK089502 · NIDDK · JOHNS HOPKINS UNIVERSITY · PI ZACHOS, NICHOLAS CONSTANTINE · 2011 to 2020
$12.0M
Molecular Mechanisms of ATP-dependent Copper TransportersR01DK071865 · NIDDK · OREGON HEALTH & SCIENCE UNIVERSITY · PI SVETLANA LUTSENKO · 2005 to 2026
$7.9M
Inductively Coupled Plasma Mass Spectrometer for High Sensitivity Elemental AnalysisS10OD028492 · OD · OREGON HEALTH & SCIENCE UNIVERSITY · PI RALLE, MARTINA · 2021 to 2021
$336k
NCATS NIH HHS UL1 TR003098NCI NIH HHS P30 CA006973NIDDK NIH HHS P30 DK089502NIDDK NIH HHS R01 DK071865NIH HHS S10 OD028492
6 · The paper itself

Abstract

objectivesAdipocyte fate determination is tightly regulated by extrinsic signaling pathways and intrinsic metabolic and morphologic changes that maintain adipose tissue function. Copper (Cu) homeostasis is required for the normal metabolism of mature adipocytes, whereas the role of Cu in adipogenesis is unclear.

methodsTo determine the role of Cu is adipocytes differentiation, we used 3T3-L1 adipocytes, immunocytochemistry, X-ray fluorescence, mass-spectrometry, pharmacological treatments, and manipulations of copper levels.

resultsIn differentiating 3T3-L1 cells, adipogenic stimuli trigger the upregulation and trafficking of the Cu transporter Atp7a, thus causing Cu redistribution from the cytosol to vesicles. Disrupting Cu homeostasis by the deletion of Atp7a results in Cu elevation and inhibition of adipogenesis. The upregulation of C/EBPβ, an initial step of adipogenesis, is not affected in Atp7a

conclusionsCu buffering during early adipogenesis contributes to termination of β-catenin signaling. Abnormal upregulation of β-catenin was also observed in vivo in the livers of Atp7b

Indexed as

Adipogenesisbeta CateninWnt Signaling PathwayAdipose TissueAnimalsCopperCopper-Transporting ATPasesHumansMicePeptide FragmentsATP7A protein, humanATP7A protein, human (2-79)beta CateninCopperCopper-Transporting ATPasesPeptide FragmentsAdipocytesATP7ACopperβ-catenin

Identifiers

PMID38185452
PMCPMC10827583
OpenAlexW4390630011

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.